Evaluation of the modulatory role of nimodipine in seizures with
kainic acid and pentylenetetrazole

R, Shitak; Sahai, Amit; Hota, Debasish; Chakrabarti, Amitava

doi:10.1358/mf.2007.29.1.1063489

Cited by 10 publications

(7 citation statements)

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“…In the present study PTZ was used to induce convulsions owing to the role of calcium ion as a common mediator in PTZ-induced convulsions [22]. This model was suitable for testing our hypothesis that the anti-convulsant activity of B. diffusa roots might be due to calcium channel blocking effect by liriodendrin.…”

Section: Discussionmentioning

confidence: 99%

Anti‐Convulsant Activity of Boerhaavia diffusa: Plausible Role of Calcium Channel Antagonism

Kaur

Goel

2011

Evidence-Based Complementary and Alternative Medicine

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“Ethnopharmacological” use of roots of Boerhaavia diffusa (B. diffusa) in the treatment of epilepsy in Nigerian folk medicine and reports showing the presence of a calcium channel antagonistic compound “liriodendrin” in its roots, led us to undertake the present study. The study was designed to investigate the methanolic root extract of B. diffusa and its different fractions including liriodendrin-rich fraction for exploring the possible role of liriodendrin in its anti-convulsant activity. Air-dried roots of B. diffusa were extracted with methanol by cold maceration. The methanol soluble fraction of extract thus obtained was successively extracted to obtain liriodendrin-rich fraction and two side fractions, that is, chloroform fraction and phenolic compound fraction. Anti-convulsant activity of methanolic extract (1000, 1500 and 2000 mg kg−1, intraperitoneally (i.p.)) and its different fractions, that is, liriodendrin-rich fraction (10, 20 and 40 mg kg−1, i.p., chloroform fraction (20 mg kg−1, i.p.) and phenolic compound fraction (1 mg kg−1, i.p.) were studied in pentylenetetrazol (PTZ)-induced seizures (75 mg kg−1, i.p.). The crude methanolic extract of B. diffusa and only its liriodendrin-rich fraction showed a dose-dependent protection against PTZ-induced convulsions. The liriodendrin-rich fraction also showed significant protection against seizures induced by BAY k-8644. These findings reiterated the anti-convulsant activity of methanolic extract of B. diffusa roots. Furthermore, it can be concluded that the observed anti-convulsant activity was due to its calcium channel antagonistic action as this activity was retained only in the liodendrin-rich fraction, which has additionally been confirmed by significant anti-convulsant activity of liriodendrin-rich fraction in BAY k-8644-induced seizures.

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Section: Discussionmentioning

confidence: 99%

Anti‐Convulsant Activity of Boerhaavia diffusa: Plausible Role of Calcium Channel Antagonism

Kaur

Goel

2011

Evidence-Based Complementary and Alternative Medicine

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“…Evidence for a role of Ca 2+ in epileptogenesis has been shown in hippocampal slices and cultured hippocampal neurons [35], [36]. Furthermore, pharmacological studies on anticonvulsant properties of Ca 2+ antagonists in mouse have provided a direct link between Ca 2+ channel function and susceptibility to PTZ-induced seizures [37]. Concerning the pharmacological actions of PF, it was reported that PF treatment suppressed the [Ca 2+ ] i elevation induced by glutamate stimulation in rat pheochromocytoma (PC12) cells [38].…”

Section: Discussionmentioning

confidence: 99%

Anticonvulsive Effect of Paeoniflorin on Experimental Febrile Seizures in Immature Rats: Possible Application for Febrile Seizures in Children

et al. 2012

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Febrile seizures (FS) is the most common convulsive disorder in children, but there have been no clinical and experimental studies of the possible treatment of FS with herbal medicines, which are widely used in Asian countries. Paeoniflorin (PF) is a major bioactive component of Radix Paeoniae alba, and PF-containing herbal medicines have been used for neuromuscular, neuropsychiatric, and neurodegenerative disorders. In this study, we analyzed the anticonvulsive effect of PF and Keishikashakuyaku-to (KS; a PF-containing herbal medicine) for hyperthermia-induced seizures in immature rats as a model of human FS. When immature (P5) male rats were administered PF or KS for 10 days, hyperthermia-induced seizures were significantly suppressed compared to control rats. In cultured hippocampal neurons, PF suppressed glutamate-induced elevation of intracellular Ca2+ ([Ca2+]i), glutamate receptor-mediated membrane depolarization, and glutamate-induced neuronal death. In addition, PF partially suppressed the elevation in [Ca2+]i induced by activation of the metabotropic glutamate receptor 5 (mGluR5), but not that mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid (AMPA) or N-methyl-D-aspartate (NMDA) receptors. However, PF did not affect production or release of γ-aminobutyric acid (GABA) in hippocampal neurons. These results suggest that PF or PF-containing herbal medicines exert anticonvulsive effects at least in part by preventing mGluR5-dependent [Ca2+]i elevations. Thus, it could be a possible candidate for the treatment of FS in children.

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“…Altered Ca2+ removal rate was also reported for animal models for epilepsy (Pal et al., 2001; Raza et al., 2001). Furthermore, pharmacologic tests with antiseizure properties of Ca 2+ antagonists and genetic mouse models have provided a direct link between Ca 2+ channels and PTZ‐induced seizure activity (Weiergräber et al., 2006; Shitak et al., 2007). Following the influx, calcium is being removed from the cell via an ATP‐dependent calcium transporter.…”

Section: Discussionmentioning

confidence: 99%

Complete brain‐type creatine kinase deficiency in mice blocks seizure activity and affects intracellular calcium kinetics

et al. 2009

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SUMMARYPurpose: Brain-type creatine kinase (CK-B) and ubiquitous mitochondrial creatine kinase (UbCKmit) act as components of local phosphocreatine-ATP shuttles that help in the compartmentalization and maintenance of pools of highenergy phosphate molecules in both neurons and glial cells. We investigated the role of these braintype creatine kinases during extreme energydemanding conditions in vivo (generalized tonicclonic seizures) and in vitro. Methods: The physiologic response of wild-types and mice lacking both CK-B and UbCKmit (CK--/--mice) to pentylenetetrazole (PTZ)-induced seizures was measured using electroencephalography (EEG) recordings and behavioral monitoring. In vitro intracellular Ca 2+ kinetics in hippocampal granule neurons were monitored upon single and repetitive depolarizations. Results: PTZ induced in only a few CK--/--mice PTZ seizure-like behavior, but in all wild-types a full-blown seizure. EEG analysis showed that preseizure jerking was associated with highamplitude discharges. Wild-type EEG recordings showed continuous runs of rhythmic 4-6 Hz activity, whereas no rhythmic EEG activities were observed in the few CK--/--mice that developed a behavioral seizure. All other CK--/--mice displayed a sudden postictal depression without any development of a generalized seizure. Hippocampal granule neurons of CK--/--mice displayed a higher Ca 2+ removal speed following repetitive KCl-induced depolarizations. Discussion: Deficiency for creatine kinase is affecting brain energy metabolism and will likely contribute to the disturbance of seizure development. Because CK--/--hippocampal neurons exhibited an increase in Ca 2+ removal rate of elevated intracellular levels, we conclude that altered Ca 2+ clearance in CK--/--neurons could play a role in the abnormal EEG and seizure activity.

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Evaluation of the modulatory role of nimodipine in seizures with kainic acid and pentylenetetrazole

Cited by 10 publications

References 0 publications

Anti‐Convulsant Activity of Boerhaavia diffusa: Plausible Role of Calcium Channel Antagonism

Anti‐Convulsant Activity of Boerhaavia diffusa: Plausible Role of Calcium Channel Antagonism

Anticonvulsive Effect of Paeoniflorin on Experimental Febrile Seizures in Immature Rats: Possible Application for Febrile Seizures in Children

Complete brain‐type creatine kinase deficiency in mice blocks seizure activity and affects intracellular calcium kinetics

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